Recent conferences revealed that tau is most toxic in oligomeric form, that tau oligomers propagate throughout the brain, and that tau oligomers might harm synapses from within or via astrocytes.
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Disrupting circadian clocks in astrocytes and microglia unleashed harmful responses in these glial cells, leading to neuronal damage.
By marrying iPSCs, human genomic data, and analysis of postmortem tissue, researchers tied loss of GABAergic signaling to tauopathies such as FTD and PSP, but not AD.
An ultrasensitive assay picked up elevated concentrations of N-terminal tau fragments in the blood of people with AD.
Cryo-EM helps explain how the inhibitory receptors open and close their ion channels.
Absent the receptor, microglia ignore Aβ seeds and new plaques, which then absorb little ApoE and stay diffuse.
Stakeholders have until February 11 to comment on draft FDA guidance for biomarker qualification.
In neurons derived from FTD patients, microtubules distort the nucleus, warping its normally rounded membrane and disrupting communication with the cytoplasm.
In familial Alzheimer’s disease, rise in NfL in the blood precedes disease onset by 16 years.
Frail people may be more likely to have Aβ plaques and neurofibrillary tangles; when they do, they are more likely to have dementia. Physical activity correlated with better global cognition, regardless of brain pathology.
Reducing systolic blood pressure staves off cognitive decline, but what about dementia?
The FDA has prioritized review of C2N’s blood test for amyloid-β. A pivotal clinical trial will correlate the test with amyloid PET scans.
At AAIC, scientists said that alterations in how the aging female brain uses energy and metabolizes fat may leave APOE4 carriers particularly susceptible to tau pathology.
New work implicates changes in chromatin structure and failed DNA repair in neurodegeneration.